Roles of interferon regulatory factor 4 in the AKI-CKD transition, glomerular diseases and kidney allograft rejection

Song, Jianling; Ke, Ben; Tu, Weiping; Fang, Xiangdong

doi:10.1080/0886022x.2023.2259228

Cited by 2 publications

(3 citation statements)

References 104 publications

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“…This occurrence might be linked to the expression of transforming growth factor-β (TGF-β), a pro-fibrotic factor, by M2 macrophages [ 55 ]. In the section discussing the AKI-CKD transition, deficiency of IRF4 impedes the AKI-CKD transition by restraining macrophage-to-fibroblast transformation, inhibiting macrophage M1-M2 polarization, and reducing inward neutrophil flow [ 129 ]. The crucial involvement of endothelin-1 in tissue fibrosis has been extensively established [ 130 ].…”

Section: Macrophages (M1/m2) Plasticity and Regulation In Clinical Re...mentioning

confidence: 99%

Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics

Islamuddin,

Qin

2024

Cell Death Discov.

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Macrophages are exceptionally diversified cell types and perform unique features and functions when exposed to different stimuli within the specific microenvironment of various kidney diseases. In instances of kidney tissue necrosis or infection, specific patterns associated with damage or pathogens prompt the development of pro-inflammatory macrophages (M1). These M1 macrophages contribute to exacerbating tissue damage, inflammation, and eventual fibrosis. Conversely, anti-inflammatory macrophages (M2) arise in the same circumstances, contributing to kidney repair and regeneration processes. Impaired tissue repair causes fibrosis, and hence macrophages play a protective and pathogenic role. In response to harmful stimuli within the body, inflammasomes, complex assemblies of multiple proteins, assume a pivotal function in innate immunity. The initiation of inflammasomes triggers the activation of caspase 1, which in turn facilitates the maturation of cytokines, inflammation, and cell death. Macrophages in the kidneys possess the complete elements of the NLRP3 inflammasome, including NLRP3, ASC, and pro-caspase-1. When the NLRP3 inflammasomes are activated, it triggers the activation of caspase-1, resulting in the release of mature proinflammatory cytokines (IL)-1β and IL-18 and cleavage of Gasdermin D (GSDMD). This activation process therefore then induces pyroptosis, leading to renal inflammation, cell death, and renal dysfunction. The NLRP3–ASC–caspase-1–IL-1β–IL-18 pathway has been identified as a factor in the development of the pathophysiology of numerous kidney diseases. In this review, we explore current progress in understanding macrophage behavior concerning inflammation, injury, and fibrosis in kidneys. Emphasizing the pivotal role of activated macrophages in both the advancement and recovery phases of renal diseases, the article delves into potential strategies to modify macrophage functionality and it also discusses emerging approaches to selectively target NLRP3 inflammasomes and their signaling components within the kidney, aiming to facilitate the healing process in kidney diseases.

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Section: Macrophages (M1/m2) Plasticity and Regulation In Clinical Re...mentioning

confidence: 99%

Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics

Islamuddin,

Qin

2024

Cell Death Discov.

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“…Moreover, it can promote macrophage polarization toward the M2 phenotype and macrophage apoptosis, reduce macrophage migration and inflammatory factor expression, induce fibrosis, as well as negatively regulate TLR-related pathways. Furthermore, it promotes the maturation of Th17 cells and maintains an inflammatory state of the tissue by T cell-derived IL-17 (198).…”

Section: Irf4 Affects the Lungs And Kidneys By Regulating Macrophage ...mentioning

confidence: 99%

“…The M2 state of macrophages also promotes fibrosis of renal tissue, which is one of the core mechanisms of AKI-CKD (198).…”

Section: Irf4 Affects the Lungs And Kidneys By Regulating Macrophage ...mentioning

confidence: 99%

Intestinal homeostasis in the gut-lung-kidney axis: a prospective therapeutic target in immune-related chronic kidney diseases

Liu,

Wang,

Zhang

et al. 2023

Front. Immunol.

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In recent years, the role of intestinal homeostasis in health has received increasing interest, significantly improving our understanding of the complex pathophysiological interactions of the gut with other organs. Microbiota dysbiosis, impaired intestinal barrier, and aberrant intestinal immunity appear to contribute to the pathogenesis of immune-related chronic kidney diseases (CKD). Meanwhile, the relationship between the pathological changes in the respiratory tract (e.g., infection, fibrosis, granuloma) and immune-related CKD cannot be ignored. The present review aimed to elucidate the new underlying mechanism of immune-related CKD. The lungs may affect kidney function through intestinal mediation. Communication is believed to exist between the gut and lung microbiota across long physiological distances. Following the inhalation of various pathogenic factors (e.g., particulate matter 2.5 mum or less in diameter, pathogen) in the air through the mouth and nose, considering the anatomical connection between the nasopharynx and lungs, gut microbiome regulates oxidative stress and inflammatory states in the lungs and kidneys. Meanwhile, the intestine participates in the differentiation of T cells and promotes the migration of various immune cells to specific organs. This better explain the occurrence and progression of CKD caused by upper respiratory tract precursor infection and suggests the relationship between the lungs and kidney complications in some autoimmune diseases (e.g., anti-neutrophil cytoplasm antibodies -associated vasculitis, systemic lupus erythematosus). CKD can also affect the progression of lung diseases (e.g., acute respiratory distress syndrome and chronic obstructive pulmonary disease). We conclude that damage to the gut barrier appears to contribute to the development of immune-related CKD through gut-lung-kidney interplay, leading us to establish the gut-lung-kidney axis hypothesis. Further, we discuss possible therapeutic interventions and targets. For example, using prebiotics, probiotics, and laxatives (e.g., Rhubarb officinale) to regulate the gut ecology to alleviate oxidative stress, as well as improve the local immune system of the intestine and immune communication with the lungs and kidneys.

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Roles of interferon regulatory factor 4 in the AKI-CKD transition, glomerular diseases and kidney allograft rejection

Cited by 2 publications

References 104 publications

Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics

Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics

Intestinal homeostasis in the gut-lung-kidney axis: a prospective therapeutic target in immune-related chronic kidney diseases

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